Glaucoma due to elevated episcleral venous pressure
Introduction
Introduction to glaucoma caused by elevated upper scleral venous pressure Maintaining a normal atrial dynamics balance and intraocular pressure depends mainly on three factors in the aqueous humor cycle, namely the rate at which the ciliary body produces aqueous humor, the rate at which aqueous humor flows out through the trabecular meshwork, and the upper scleral venous pressure. The maintenance of intraocular pressure level depends on the dynamic balance of the three. Glaucoma caused by elevated upper scleral venous pressure is not uncommon in clinical practice, but the cause is complicated and the treatment effect is also poor. basic knowledge The proportion of illness: 0.002% Susceptible people: no special people Mode of infection: non-infectious Complications: neovascular glaucoma
Cause
Causes of glaucoma caused by elevated upper scleral venous pressure
(1) Causes of the disease
Any cause of blood flow obstruction or abnormal blood flow in the upper scleral vein or iliac vein system can eventually cause elevation of the upper scleral venous pressure and block the outflow of aqueous humor. The increase in intraocular pressure leads to glaucoma. The common clinical causes are as follows. Several aspects:
1. Venous blood return disorder: local iliac vein or total body venous system - superior vena cava reflux disorder can cause obstruction of upper scleral venous blood flow, upper scleral venous pressure rises and glaucoma, local venous venous return obstruction is common in Severe Grave disease (infiltration of inflammatory cells, hyperplasia and edema, extraocular muscle swelling caused by ocular swelling, iliac vein congestion, reflux obstruction); venous system - superior vena cava blood return disorder is common in aortic aneurysm, mediastinal tumor, central Type of lung cancer, scarring mediastinal inflammation, hilar lymphadenopathy, ectopic goiter, etc. directly compress the superior vena cava, causing obstruction of the blood flow in the superior vena cava system, clinically showing typical superior vena cava syndrome, in the local Among the factors, the tumor in the posterior part of the ball can also compress the apical vein to prevent the venous venous return. However, due to the extensive traffic branch of the iliac vein, the tumor after the ball is less likely to cause the whole iliac vein blood flow to be blocked and lead to glaucoma.
2. Abnormal venous blood flow (arterio-venous fistula): due to abnormal traffic of arteries and veins, arterial blood flows into the iliac vein, causing increased venous pressure and venous blood flow. Common causes are internal carotid artery-spontaneous sinus Sputum and dural arterial-cavernous sinus fistula (red eye short circuit syndrome), the former is particularly common, the cause is mostly traumatic skull base fracture, caused by congenital or atherosclerotic aneurysm rupture.
Clinically, patients with arteriovenous fistula show typical pulsatile eyeballs. Patients complain of pulsating tinnitus, vascular murmurs can be heard in the ear, pulsating eyes in the eyes, high edema of the eyelids and conjunctiva, and upper sclera. The veins are obviously filled and distorted, the retinal veins of the fundus are engorged, the eyes and eyelids are lowered when the head is lowered, the conjunctival edema is aggravated, and the eyeballs can be relieved when the eyeball is continuously pressed or the ipsilateral or the common carotid artery is compressed. The eye palpation has a cat. "Heavy sensation", the eye auscultation can smell vascular murmur.
The treatment of patients with arteriovenous fistula is mainly surgical treatment, and is assisted by brain surgery and vascular surgery. The surgical methods mainly include carotid artery ligation through the neck and intracranial and extracranial carotid ligation. Intravenous pupillary embolization, etc., a small number of patients with low-flow dural arteriospora fistula due to low blood flow, low pressure, blood vessel rupture can form a self-contained thrombus obstruction and self-healing.
3. Internal varicose veins: Orbital varicose veins can also block the venous venous return, the upper scleral venous pressure is increased secondary to glaucoma, orbital varices have primary and secondary, primary orbital veins Congenital varicose and thin wall, may be associated with scalp and intracranial varicose veins, but not with intraorbital and intracranial arteriovenous malformations or arteriovenous fistula; secondary is often secondary to intraorbital or cranial Internal arteriovenous fistula, secondary dilatation of the orbital vein or arteriosclerosis, of which the most common varicose veins in the eye, clinically, intra-orbital varices showed intermittent eyeballs.
4. Hemangioma: congenital eyelids and (or) facial hemangioma (can be combined with intracranial hemangioma), may be accompanied by elevated upper scleral venous pressure and secondary glaucoma, namely Sturge-Weber syndrome.
5. Idiopathic (spontaneous) upper scleral venous pressure: This type of patient has clinical manifestations similar to primary open angle glaucoma, accompanied by superficial scleral vasoconstriction and superior scleral venous pressure on the surface of the eye. Elevated, but can not find the cause of the increase in the upper scleral venous pressure, the mechanism is still unclear, can be unilateral or bilateral, with a family-onset tendency, clinically easy to be confused with primary open-angle glaucoma Should pay attention to the differential diagnosis.
(two) pathogenesis
The cause of glaucoma caused by increased upper scleral venous pressure may be the result of the following effects:
1. Upper scleral venous pressure: When the upper scleral venous pressure rises above the intraocular pressure level, the blood flows back into the Schlemm tube, and the plasma protein in the blood has a higher colloid osmotic pressure and an increase in the Schlemm lumen. The colloid osmotic pressure counteracts the pressure gradient existing between the anterior chamber and the Schlemm tube, so that the aqueous humor enters the Schlemm tube through the iris corneal trabecular meshwork, and the aqueous humor flow is close to zero, causing an increase in intraocular pressure. Clinically, intraocular pressure imaging examination of glaucoma caused by elevated upper scleral venous pressure can be found that the C value of aqueous humor flow coefficient is significantly reduced.
2. Vortex venous return is blocked: Vortex venous return is blocked, venous pressure is increased, uveal membrane is congested, swelling, anterior chamber volume is reduced, iris corneal angle is narrowed and anterior adhesion around the iris, leading to iris keratoconus closure and secondary closure Angle glaucoma.
3. Increased venous pressure: reduce intraocular perfusion pressure, resulting in optic disc blood supply disorders, glaucoma optic disc and visual function damage as a result of optic disc ischemia, this part of the patient may still have central retinal vein occlusion.
Prevention
Glaucoma prevention caused by elevated upper scleral venous pressure
There is no effective preventive measure for this disease. Early detection and early diagnosis are the key to the prevention and treatment of this disease.
Complication
Glaucoma complications caused by elevated upper scleral venous pressure Complications, neovascular glaucoma
Typical glaucomatous optic disc damage occurs, and neovascular glaucoma can occur in the advanced stage.
Symptom
Symptoms of glaucoma caused by elevated upper scleral venous pressure Common symptoms Pulsating tinnitus Retinal edema Hairy red eyes Congestive eyeballs High eye pressure Dizziness Convulsion Double vision
1. General clinical features:
(1) ocular surface: the affected eye has different degrees of superficial scleral blood vessels and conjunctival vasodilatation, similar to congestion, and in some cases, the subcutaneous blood vessels of the eyelids are obviously varicose, which may be accompanied by eyeballs and even eyeballs.
(2) Intraocular pressure: The increase of intraocular pressure is similar to the increase of superficial scleral venous pressure. It is usually higher in the supine position, but the increase in intraocular pressure can be greatly exceeded in the long-term superficial scleral venous pressure. The value of elevation of the scleral venous pressure.
(3) Corner: The angle of the keratoscopy is an open angle. It is often seen that the Schlemm tube is congested. It is caused by the increase of superficial scleral venous pressure, which can be seen in normal eyes. Especially when the angle of the gonioscopic examination oppresses the eyeball, the diagnosis of the increase of the surface scleral venous pressure is only of reference value.
(4) Intraocular pressure tracing: the general aqueous humor flow coefficient (C value) is normal when the surface scleral venous pressure is increased, and the C value may increase in the early stage, which is caused by the partial expansion of the Schlemm tube, but the long-term surface scleral venous pressure is increased. In the case of C, the C value is often lowered, that is, the C value is still at a lower level after the recovery of the surface scleral venous pressure, which is caused by the continuous elevation of the superficial scleral venous pressure causing damage to the aqueous outflow tube system.
(5) fundus: manifested as typical glaucomatous optic disc damage, corresponding to glaucomatous visual field damage, increased central retinal vein showed varying degrees of dilated tortuosity, which can lead to central retinal vein thrombosis and secondary neovascular glaucoma.
2. Common types and clinical features of secondary glaucoma:
Increased superficial scleral venous pressure secondary to glaucoma, and some cases with characteristic clinical manifestations, easy to diagnose, such as vena cava syndrome and severe arteriovenous fistula, and some cases need to be carefully observed.
(1) superior vena cava syndrome: when the upper mediastinal lesion is blocked by the superior vena cava, it can cause superior vena cava syndrome. The initial symptoms are mild edema of the eyelid, conjunctival and superficial scleral vein filling, followed by eyeball protrusion, face, Cervical edema and cyanosis, causing increased intracranial pressure, headache, dizziness and even convulsions, increased visceral venous pressure and elevated intraocular pressure in the eye, elevated intraocular pressure than sitting position, central retinal vein It is characterized by distorted dilatation and retinal edema. As the intracranial pressure increases, the glaucoma sag of the optic disc is often not obvious.
(2) carotid-cavernous sinus fistula: the most common in arteriovenous fistula, typical carotid-cavernous sinus fistula occurs after head trauma, the characteristic manifestation is pulsatile eyeball with pulsating tinnitus murmur And eyelid pain, obstruction of venous system blood flow causes orbital vein and soft tissue congestion, eyelid and conjunctival edema, superficial scleral varicose veins, central retinal veins with varying degrees of dilated tortuosity, retinal edema, exudation, around the eyelids Blood flow noise can be heard. When the internal carotid artery is compressed, the sound is weakened. In typical cases, the blood vessels in the eye can be pulsated in the eye. Due to the decrease of intraocular perfusion pressure, the visual acuity can be significantly reduced and the ocular ischemic syndrome is complicated. About half of the cases have double vision, and 1/3 of the cases have eye pain. Because of the intracranial traffic of the cavernous sinus on both sides, one side of the carotid-cavernous sinus can cause bilateral or alternating pulsatile eyeballs, and the other type is Atypical spontaneous carotid-cavernous sinus fistula, mostly in middle-aged and old women, no history of trauma, manifested as superficial scleral vein and conjunctival vein expansion, eyeball protrusion is not obvious Non-pulsatile tinnitus, this type of short circuit known as red-eye syndrome, also known as the dura syndrome.
About 60% of carotid-cavernous fistula cases have elevated intraocular pressure. The mechanism of secondary glaucoma is: carotid-cavernous sinus arterial blood mixed with venous blood, iliac venous pressure and superficial scleral venous pressure , resulting in increased intraocular pressure, in addition, carotid-cavernous sinus fistula vortex venous pressure increased, the entire uveal membrane congestion, followed by pupillary block, angle closure caused by acute angle-closure glaucoma; or due to reduced arterial blood flow, resulting in Ocular ischemia, causing uveal inflammatory response, secondary to anterior corner damage; or causing redness of the iris, leading to neovascular glaucoma.
(3) sacral varices: the disease is unilateral, congenital or secondary to the sacral, intracranial arteriovenous fistula or from hemangioma, characterized by intermittent eyeballs, generally in the body When the head bows or Valsalva moves, the eyeballs are mostly invaginated during the intermittent period. The patient's eyelids and varicose veins are visible in the front of the eyelids. The X-ray film is enlarged by the eyelids. The B-mode ultrasound image shows the gap of the liquid density after the ball. CT examination The varicose veins showed a soft tissue mass. The angiography was negative. The venous angiography showed vascular malformation. The superficial scleral venous pressure of the two eyeballs was normal. Therefore, secondary glaucoma rarely occurred, but repeated eyeballs protruded. Increased scleral venous pressure can also occur glaucomatous optic disc disease and visual field damage. In most cases, visual function prognosis is better.
(4) Sturge-Weber syndrome: also known as facial hemangioma syndrome, is an early vascular developmental malformation of congenital embryos, and the tumor and cerebral vessels are abnormally dilated, showing a grape-like purple-red skin along the trigeminal nerve distribution area. Hemangioma, 50% of cases can involve intracranial and glaucoma, hemangioma involving the eyelids, regardless of the intracranial or not, may be accompanied by elevated scleral venous pressure and secondary glaucoma, especially involving the palate Glaucoma can occur at any age, but most of it can be seen in childhood. It can have "bull-eye" performance. Almost all patients with glaucoma have superficial scleral hemangioma, as well as anterior chamber and choroidal hemangioma. In addition, affected The iris color is dark, occasionally retinal varices, and the intraocular pressure can be significantly increased in the supine position. Some eyes only see diffuse scleral hemangioma after opening the fascia during surgery. Glaucoma is mostly caused by superficial scleral vein. Due to the increase in pressure, in some cases, there may be obvious factors such as the angle of the anterior chamber and the anterior chamber angle caused by choroidal hemangioma.
(5) Thyroid-associated ophthalmopathy: also known as Graves' ophthalmopathy, invasive exophthalmos, thyroid-associated immunological eyelids, etc., is the most common cause of eye protrusion in both eyes and eyes of adults. Pathological changes are mainly extraocular muscle edema, lymphocytes Infiltration, muscle degeneration and necrosis and fibrosis, post-balloon fat and connective tissue fibroblasts are active, mucopolysaccharide deposition and edema. Clinical manifestations include upper eyelid retraction and eyeball protrusion, diplopia and eye movement limitation, due to frequent companion The sputum congestion, infiltration and extraocular muscle hypertrophy and the tension of the eyelid retraction, so that the pressure in the eyelids increases, which can cause the increase of superficial scleral venous pressure, leading to glaucomatous visual function damage. This disease is often accompanied by a decrease in the hardness of the ball wall. The applanation tonometer measures intraocular pressure, but different eye positions can cause significant differences in measured intraocular pressure, especially when the eyeball is gazing upwards, which is accompanied by an increase in intraocular pressure. In addition, attention is paid to the extraocular muscles that are excessively hypertrophied at the tip of the eye. Can cause oppressive optic neuropathy.
(6) Idiopathic superficial scleral venous pressure: more common in the elderly, can also occur in young patients, family-oriented, the disease process is similar to the primary open angle glaucoma, but the surface scleral venous pressure is significantly increased The fluency coefficient of aqueous humor is often reduced. There may or may not be blood in the Schlemm tube. Most cases are unilaterally involved. Serious glaucomatous damage may eventually occur. The cause of elevated scleral venous pressure is unknown. The trabeculectomy specimen shows Close to the Schlemm tube trabecular layer is compressed and has extracellular deposition and trabecular tissue glassy changes, but it is difficult to judge whether this is primary or secondary.
Examine
Examination of glaucoma caused by elevated upper scleral venous pressure
Perform necessary laboratory tests such as TT3, TT4, FT3, FT4 and TRH for primary diseases such as thyroid-related eye diseases.
1. Visual field examination: indicates the severity of glaucomatous visual field damage.
2. Intraocular pressure tracing: Observing changes in C value is an important reference for estimating the condition.
3. Intraocular pressure measurement.
Diagnosis
Diagnosis and diagnosis of glaucoma caused by elevated upper scleral venous pressure
1. The patient has a primary disease that causes an increase in the superior scleral venous pressure.
2. The upper scleral venous pressure is elevated.
3. High intraocular pressure, glaucomatous optic disc damage and visual field damage, iris corneal angle can be wide, open angle or iris corneal angle adhesion closure.
For glaucoma secondary to elevated upper scleral venous pressure, there are two cases that are easily overlooked by clinicians. First, when patients have primary diseases that can cause elevated upper scleral venous pressure, only the diagnosis and treatment of primary disease are noted. While neglecting the possible presence of glaucoma, therefore, when there is a primary disease that can cause elevation of the upper scleral venous pressure, the intraocular pressure should be routinely measured, and if there is an increase in intraocular pressure, the iris cornea angle, optic disc and visual field should be further examined. To confirm the diagnosis, the second case is glaucoma secondary to idiopathic upper scleral venous pressure. Because its clinical manifestations are similar to those of primary open angle glaucoma, if you do not examine the superficial scleral vein carefully, it is often easy to ignore. The manifestation of elevated scleral venous pressure was misdiagnosed as primary open angle glaucoma.
